New findings by scientists at the University of California, Santa Cruz (UC Santa Cruz), suggest that an evolutionary arms race between rival elements within the genomes of primates drove the evolution of complex regulatory networks that orchestrate the activity of genes in every cell of our bodies. The arms race is between mobile DNA sequences known as "retrotransposons" (also known as "jumping genes") and the genes that have evolved to control them. The UC Santa Cruz researchers have, for the first time, identified genes in humans that make repressor proteins to shut down specific jumping genes. The researchers also traced the rapid evolution of the repressor genes in the primate lineage. Their findings, published online on September 28, 2014 in Nature, show that, over evolutionary time, primate genomes have undergone repeated episodes in which mutations in jumping genes allowed them to escape repression, which drove the evolution of new repressor genes, and so on. Furthermore, their findings suggest that repressor genes that originally evolved to shut down jumping genes have since come to play other regulatory roles in the genome. "We have basically the same 20,000 protein-coding genes as a frog, yet our genome is much more complicated, with more layers of gene regulation. This study helps explain how that came about," said Dr. Sofie Salama, a research associate at the UC Santa Cruz Genomics Institute who led the study. Retrotransposons are thought to be remnants of ancient viruses that infected early animals and inserted their genes into the genome long before humans evolved. Now they can only replicate themselves within the genome. Depending on where a new copy gets inserted into the genome, a jumping event can disrupt normal genes and cause disease.

Collaborating scientists at Dana-Farber Cancer Institute, the Massachusetts Institute of Technology (MIT), and other institutions have discovered a sign of the early development of pancreatic cancer – an upsurge in certain amino acids that occurs before the disease is diagnosed and symptoms appear. The research is being published online on September 28, 2014 in Nature Medicine. Although the increase isn't large enough to be the basis of a new test for early detection of the disease, the findings will help researchers better understand how pancreatic cancer affects the rest of the body, particularly how it can trigger the sometimes deadly muscle-wasting disease known as cachexia. "Most people with pancreatic ductal adenocarcinoma (PDAC) (by far the most common form of cancreatic cancer) are diagnosed after the disease has reached an advanced stage, and many die within a year of diagnosis," said Brian Wolpin, M.D., M.P.H., of Dana-Farber, co-senior author of the new study with Matthew Vander Heiden, M.D., Ph.D., of MIT and Dana-Farber. "Detecting the disease earlier in its development may improve our ability to treat it successfully. In this study, we asked whether PDAC produces metabolic changes – changes in the way the body uses energy and nutrients – that can be detected before the disease is diagnosed." The researchers utilized blood samples collected years earlier from 1,500 people participating in large health-tracking studies. The scientists analyzed the samples for more than 100 different metabolites – substances produced by the metabolic process – and compared the results from participants who had gone on to develop pancreatic cancer and those who had not.

National Institutes of Health (NIH) and Colorado State University (CSU) scientists have provided experimental evidence supporting dromedary camels as the primary reservoir, or carrier, of Middle East respiratory syndrome coronavirus (MERS-CoV). The study, designed by scientists from CSU and NIH's National Institute of Allergy and Infectious Diseases (NIAID), involved three healthy camels exposed through the eyes, nose, and throat to MERS-CoV isolated from a patient. Each camel developed a mild upper respiratory tract infection consistent with what scientists have observed throughout the Middle East. Samples taken from the camels showed high levels of infectious virus in secretions, primarily from the nose, for up to a week after infection; the scientists detected components of the virus for up to 35 days. Although the camels quickly recovered from infection without apparent complications, the researchers say the nasal secretions provide a likely source of transmission to people who handle the animals. The researchers theorize that vaccinating camels could reduce the risk of MERS-CoV transmission to people and other camels; NIAID and others are supporting research to develop candidate vaccines for potential use in people and camels. The MERS outbreak, which began in 2012, continues throughout the Middle East. Since the outbreak began, NIAID researchers have focused on understanding how the virus causes disease and how it can be treated effectively. As of July 23, 2014, the World Health Organization has reported a total of 837 human cases of MERS-CoV infection, including at least 291 deaths. The open-access article describing the current study was published online, ahead of print, in Emerging Infectious Diseases, produced by the CDC, and is scheduled for print publication in December 2014.